Posts Tagged ‘hypothalamus’


Migraines (Part 4) (Last Edited: 2009 Nov 19)

2008 August 23

Go back to Part 3

This is the final part of a four part series about migraine. You can use the links above or at the end of this page to go back. Or you can jump to any part from the Migraine FAQs page link.

There is difference of opinion over the exact mechanism for migraine pain. Both agree that the trigeminal nerves, that registers pain, are central to the mechanism. These relay pain signals to the thalamus. The thalamus processes them and then passes information to the cerebral cortex that registers it as pain. But the mechanism for pain signal generation in the trigeminal nerve differs between the two theories.

One school suggests that the cortical spreading depression directly stimulates the trigeminal nerves through the release of neurotransmitters and ions as the wave spreads. These then stimulate the trigeminal nerves to register pain. There is evidence supporting this mechanism, even in patients who do not necessarily experience aura during the spreading depression. This is also supported by the observation of increased, then decreased, blood flow in migraine without aura. This theory also helps explain vaguer symptoms observed such as fatigue or difficulty concentrating.

The second school places the cause of pain in the brain stem. This is the control centre for pain sensitivity, as well as other functions. Positron-emission tomography (“PET scans”) during migraine attack show that three clusters of cells called “nuclei” are active during and after migraine. This school suggests that abnormal activity here induces two pathways to pain. These nuclei normally inhibit the trigeminal nerves, reducing pain sensitivity. The nuclei’s misbehaviour may activate the trigeminal nerves causing them to fire and register “phantom pain”. It is suggested the nuclei may even trigger cortical spreading depression. These nuclei also control the flow of sensory information like light, noise and smell. Misfiring in the nuclei may explain the sensitivity to these during some migraine attacks.

There is also a minority opinion that migraine begins in neck pain.

The activity of the nuclei are also changed by behavioural and emotional states, which are also accepted as possible migraine triggers. The nuclei receive input from only two parts of the cortex; those that regulate arousal, attention and mood. These links could explain the mood fluctuations sometimes observed during migraine and the statistical association between migraine, depression and anxiety disorders.

The neurotransmitter serotonin seems to play some role in migraine. It also plays a part in mood regulation and in anxiety disorders and depression. Its role in blood vessel dilation may be important. Triggers like stress, bright lights, dehydration and so on are thought to increase serotonin levels in the brain. This disrupts the normal functioning of the hypothalamus and may trigger the blood vessel changes in migraines. Studies have shown how injection of a drug called reserpine, that releases serotonin, induces migraine headaches in sufferers, but not other people.

Both these new approaches may eventually offer relief for migraine sufferers. At present, few drugs can prevent migraine. None of the drugs used today were developed specifically for migraine. Only around one in two sufferers are helped by them and the potential side effects can be serious. Those that tend to be most effective, anti-hypertensives, anti-epileptics and antidepressants, have all been shown to inhibit cortical spreading depression. This supports the theory that this neural phenomenon contributes to migraine both with and without aura. New drugs are now in development that target “gap junctions” – a type of ion channel – effectively halting calcium flow between brain cells.

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MacGregor, Dr Anne. 2005. Understanding Migraines and Other Headaches. Family Doctor Publications Limited/British Medical Association